Evidence map›Paper›PMID 26106146›Full record

ReviewPharmacological reviews2015

Dopamine's Actions in Primate Prefrontal Cortex: Challenges for Treating Cognitive Disorders.

Amy F T Arnsten, Min Wang, Constantinos D Paspalas

Open access · bronzeAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021
    Pooled it
  3. Trial
  4. Methylphenidate undermines or enhances divergent creativity depending on baseline dopamine synthesis capacity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Trial
  5. Trial
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Neural basis for individual differences in the attention-enhancing effects of methylphenidate.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Dopamine D1 receptor in medial prefrontal cortex mediates the effects of TAAR1 activation on chronic stress-induced cognitive and social deficits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  15. Article
  16. Dynamic Network Connectivity: from monkeys to humans.Frontiers in human neuroscience · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Amy F T ArnstenDepartment of Neurobiology, Yale University School of Medicine, New Haven, Connecticut amy.arnsten@yale.edu.
Min WangDepartment of Neurobiology, Yale University School of Medicine, New Haven, Connecticut.
Constantinos D PaspalasDepartment of Neurobiology, Yale University School of Medicine, New Haven, Connecticut.
Yale University · US

Funding

Highly evolved brain circuits in primates: molecular vulnerabilities for diseaseDP1AG047744 · NIA · YALE UNIVERSITY · PI ARNSTEN, AMY F.T. · 2013 to 2017
$4.1M
NIA NIH HHS DP1 AG047744NIA NIH HHS DP1-AG047744-01
6 · The paper itself

Abstract

The prefrontal cortex (PFC) elaborates and differentiates in primates, and there is a corresponding elaboration in cortical dopamine (DA). DA cells that fire to both aversive and rewarding stimuli likely project to the dorsolateral PFC (dlPFC), signaling a salient event. Since 1979, we have known that DA has an essential influence on dlPFC working memory functions. DA has differing effects via D1 (D1R) versus D2 receptor (D2R) families. D1R are concentrated on dendritic spines, and D1/5R stimulation produces an inverted U-shaped dose response on visuospatial working memory performance and Delay cell firing, the neurons that generate representations of visual space. Optimal levels of D1R stimulation gate out "noise," whereas higher levels, e.g., during stress, suppress Delay cell firing. These effects likely involve hyperpolarization-activated cyclic nucleotide-gated channel opening, activation of GABA interneurons, and reduced glutamate release. Dysregulation of D1R has been related to cognitive deficits in schizophrenia, and there is a need for new, lower-affinity D1R agonists that may better mimic endogenous DA to enhance mental representations and improve cognition. In contrast to D1R, D2R are primarily localized on layer V pyramidal cell dendrites, and D2/3R stimulation speeds and magnifies the firing of Response cells, including Response Feedback cells. Altered firing of Feedback neurons may relate to positive symptoms in schizophrenia. Emerging research suggests that DA may have similar effects in the ventrolateral PFC and frontal eye fields. Research on the orbital PFC in monkeys is just beginning and could be a key area for future discoveries.

Indexed as

AnimalsCognition DisordersDopamineDopamine AgonistsDrug DesignHumansMemory, Short-TermPrefrontal CortexPrimatesReceptors, DopamineSchizophreniaDopamineDopamine AgonistsReceptors, Dopamine

Identifiers

PMID26106146
PMCPMC4485014
OpenAlexW2156295541

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.